Titlebook: Neuroinflammation — From Bench to Bedside; H. Kettenmann,G. A. Burton,U. J. Moenning Conference proceedings 2002 Springer-Verlag Berlin He

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,Activated Microglia in Alzheimer’s Disease and Stroke,al (Kreutzberg 1996). Under pathological conditions, microglia proliferate and transform into active “brain macrophages”. In this activated state, microglia secrete a number of inflammatory mediators including nitric oxide, glutamate, proteases, superoxide and cytokines. Thus, if micro-glia remain a

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,Inflammation in Stroke — A Potential Target for Neuroprotection?,schemic to inflammatory injury. Under normal circumstances, endothelial cells present an anti-thrombotic and anti-inflammatory surface to the blood. However, the release of chemokines and cytokines from brain-derived and circulating cells after ischemia triggers a cascade of potentially damaging eve

extemporaneous

The Concept of In Vivo Imaging of Neuroinflammation with [11C](R)-PK11195 PET, understanding of the disease process might be. The number of in vivo probes that would allow us to detect and measure the de novo expression of molecules specifically associated with those cellular changes that characterise a neuropathological tissue reaction, i.e. the “positive phenomenology” of t

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Pineal Gland and Behavior,nsistent finding following pineal manipulations. From anatomical considerations, especially in lower vertebrates, and from associated experimental studies, it was also suspected, and sometimes demonstrated, that the pineal was responsive to changes in the photic environment.

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